5. cardiac muscle Flashcards

1
Q

what is the nature of contraction

A

constant

near synchronous in ventricles

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2
Q

actions that increase the function of the heart

A

inotropy- increased force of contraction (increased SV)

chronotropy- increased frequency of contraction (increased hr)

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3
Q

myosin isoforms

A

more homologous than skm, no fibre typing

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4
Q

how are cardiac muscle cells adapted for synchronous electric activity

A

branched fibres are joined with intercalated discs and desmosomes
allow strong adherence and low resistance gap junctions allowing propagation of myocardial AP through heart

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5
Q

intercalated discs: transverse components

A
  1. desmosomes

2. fasciae adherents- antinin and vinculin

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6
Q

how does a cardiac myocyte AP differ from Skm AP

A
LONG 
refractory period (influx of calcium) 
avoids tetanic contractions
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7
Q

difference in T tubules

A

thick t tubules (vs thin in skeletal)
limited SR (vs extensive)
DIADS (vs triads)

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8
Q

EC coupling

A

plateau results from opening of L-type calcium channels
open more slowly than Na channels (of first phase of AP)
Opening of L-type delays repolarisation
only a small amount of calcium enters cell

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9
Q

where is cardiac AP propagated

A

along sarcolemma into t tubules

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10
Q

L-type channels and ryanodine receptors

A

calcium enters the L-type channels which are near ryanodine receptors
this causes calcium release by SR
enables Ca to rise a little more (less than skeletal)

calcium is then requested by SR via ATPase pumps and expelled from cell by Na-Ca exchange

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11
Q

transport proteins in sarcolemma

A

ATPase pump
Na-Ca exchanger
vg K channels
beta adrenergic receptor

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12
Q

how does calcium transient drive cardiac contraction

A

increase in diastolic length of cardiac myocyte increases sensitivity of myocyte to calcium (Starling’s law of heart)
drugs can modulate calcium transient
L-type calcium blockers- negative inotrope- beneficial in angina as reduced contraction reduces energy demands, reducing ischaemia

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13
Q

which drug lengthens calcium transient

A

digitalis/ digoxin

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14
Q

cardiac muscle and ATP

A

makes lots of ATP- lots of mitochondria
70% from oxidation of fat
20% from oxidation of glucose

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15
Q

cardiac muscle mitochondria

A

continuous reticulum:
Interfibrillar mitochondria
subsarcolemmal mitochondria

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16
Q

cardiac muscle AP

A
  1. AP arrives at opening of L-type calcium channels in plasma membrane and T tubules- Ca enters from EC fluid
  2. Ca from T tubule triggers Ca release from SR due to ryanodine receptors (75-90%)
  3. Ca pumped back into SR via Ca ATPase pump and expelled across plasma membrane by 3Na-Ca exchange exchanger is driven by Na gradient across membrane, maintained by Na/K ATPase

net eff

17
Q

Norepinephrine affect on cardiac muscle

A

binds to beta 1 adrenoreceptors on sarcolemme-> increase cAMP-> cAMP mediated phosphorylation of Ca channels increase Ca entry during AP, increase Ca release on SR

also activated Ca channels via G proteins
also cAMP mediated phosphorylation of phospholamban (activates ATPase- increased uptake so next AP can happen)

18
Q

regulator of cardiac muscle

A

only calcium